By moving from correlations to causality in cancer signal transduction using optogenetics, the sufficiency of RalB activation to trigger invasion and the underlying molecular mechanisms were established.
Differential eIF4E binding to transcription initiation nucleotides and alternative promoter usage of eIF1A, PABP and other genes are involved in the response of the translation machinery to energy stress.
Functional recapitulation of a likely evolutionary gain in gene expression shows that two genes are sufficient to switch mesoderm cell internalization from stochastic cell ingression to coordinated epithelial invagination.
The Ras activator RasGRP1 that impacts Ras signals in immune cells, leukemias, and colorectal cancer, switches to an active conformation aided by a pH-sensitive histidine residue in a central location of the RasGRP1 molecule.
Spatially and temporally patterned activation of the small GTPase Rho1 indicates that ventral-specific factors contribute to cell- and tissue-level behaviors during ventral furrow formation, the first step in Drosophila gastrulation.
The probability of a cellular response to a differentiation inducing signal is correlated with the dynamic expression of a Ras protein, and produces a ‘salt and pepper’ pattern of cell differentiation.